Hi all
Need some advice/opinions on a plan I tend to start next week, ive used both jintropin and igf-1 lr3 before as a combined cycle and it worked well.
My next cycle I was thinking along the lines of
Monday
GHRH (1295) 200mcg morning on waking up (before breakfast)
GHRP-6 100mcg morning before breakfast
Hexarelin 100mcg morning before breakfast
Midday after workout
Igf-Lr3 100mcg bi-lat
Evening
GHRP-6 100mcg before bed and last meal
Hexarelin 100mcg morning before breakfast
GHRH (1295) 200mcg before bed.
Repeat same protocol for Tuesday But NO GHRH, add in the GHRH for wednesday non thursday and Last dosage on Friday leaving the weekend off and repeating everything again on monday.
My aim is to put a little bit of mass and cut up a little more while increasing strength, AAS is out of the question as its can be traced in testing and its somthing i don't want to get into at this stage in my life.
P.S ive read comments that people dont think igf-1 is good to use while using 1295? do you think id be best just doing the Igf-1 on a cycle on its own for 2 weeks then starting the above plan without igf-1 ?
Any comments appreciated
Oops...I forgot to answer your email.
What is that it you think the IGF-1 LR3 is going to give you? It is small enough of a molecule that it will not remain in the local tissue injected into. Its binding affinity (like all long lasting analogs) is weaker then native IGF-1 so its not like a lot of it will automatically bind to receptors.
Most of that large dose will pass through capillary walls and enter the blood stream and circulate.
Only native IGF-1 + IGFBP + ALS creates a complex too large to move through vessel walls and thus if injected would remain "trapped" in extra-vascular tissue where it could serve as a pool of IGF-1 easily capable of dissassociating from the complex and binding to an available receptor when available.
Growth Hormone increases both circulating IGF-1 (derived from synthesis in the liver) AND locally produced and used IGF-1. So if you increase GH you will increase the amount of IGF-1 made & used in muscle tissue.
Why is this local producton/use different then local injection of IGF-1 (if you could keep it in target tissue)? Some of GH and IGF-1 is created & prebound to a receptor inside the cell. The complex is inactive until it rises to the cell surface where a conformational change brings into allignment certain residues within the intracellular domain of the receptor that active the signaling cascades that will mediate the events requisite for growth. In other words the ligand & receptor are birthed together so that no free IGF-1 molecule outside the cell has a chance to bind.
Naked receptors are birthed as well and locally unbound IGF-1 is created as well.
It is the locally produced & used IGF-1 that for the most part creates growth much more than liver-derived cirulating IGF-1.
The amount of GH that your chosen dosing level of CJC/GHRP will produce is not huge. If it were a really large dose I would feel confident in saying that the extra IGF-1 will be of no benefit.
But at the lower dose there will be room for extra IGF-1 action in muscle tissue.
So that leaves IGF-1 inhibition of GH release. GH & IGF-1 in circulation can feedback on the Hypothalamus and the Pituitary. Since we don't need the hypothalamus to give us GHRH (because we supply that with the CJC-1295) we are less concerned with THAT particular inhibition. We can still maintain a concern because GHRP-6 acts in part to also induce further release of GHRH from the hypothalamus but for the most part we have in our syringe THE hypothalamic hormone responsible for GH release so when we inject it, it travels directly to the pituitary and exerts it's effect.
The problem though is GH & IGF-1 inhibition at the pituitary. The somatotrophs (i.e. cells in the pituitary that release GH from internal stores) have many types of receptors on the cell membrane. Among those types is the growth hormone receptor (GHR) & IGF-1 receptor. So GH &IGF-1 in circulation can bind to a receptor on the very cells that secrete GH in the first place. When this occurs it invokes certain mechanisms that result in the somatotroph ceasing GH release.
There is nothing about our CJC-1295/GHRP-6 protocol that bypasses the negative feedback mechanisms at the pituitary. If a decent amount of systemic IGF-1 & GH is in our system some of it will bind to a receptor on the somatotroph in the pituitary and any subsequent administration of GHRH (in the form of CJC-1295) will be either without or with reduced influence or effect.
GH promotes locally produced/used IGF-1 which for the most part stays local & has not much inhibitory effect as described. However that IGF-1 LR3 that you inject will as will GH-derived liver synthesized IGF-1 .
So your 100mcg is considered substantial with a greater likelihood of inhibitory effect then a lesser amount. Only a small portion of IGF-1 LR3 has much of a chance to bind near the injection site immediately anyway. So you second hope is that the remainder which becomes circulationg IGF-1 LR3 will circulate back and bind locally. "SHANE! Come back Shane! We love you Shane! ...but he just kept riding away."
Plenty of anectdotal feedback from people who have used both CJC/GHRP & IGF-1 LR3 primarily for injury repair ...Pumertot and wophood for example... indicate that the IGF-1 LR3 has added effect.
But the effect IMHO will be less then additive. In essence 5 + 3 = 6.8 ...and a lot will depend on how you use these compounds.
Good to have you here. :head:
. I am fairly well at nutrition planning and such, but I have a few questions related to peptide usage.